Di Lorenzo G, Pacor M L, Vignola A M, Profita M, Esposito-Pellitteri M, Biasi D, Corrocher R, Caruso C
Dipartimento di Medicina Clinica e delle Patologie Emergenti, Università degli Studi di Palermo, Italy.
Allergy. 2002 Dec;57(12):1180-6. doi: 10.1034/j.1398-9995.2002.23767.x.
The recovery of mediator metabolites from urine has the potential to provide a rapid, safe, and easily available index of release of mediators. We aimed to determine urinary metabolites of both histamine and leukotrienes (LTs) in patients affected by chronic urticaria (CU).
Twenty patients with CU were studied. They were selected on the basis of double-blind placebo-controlled challenge (DBPC) with acetyl salicylic acid (ASA) and food additives. Ten patients (group B) were negative to both challenges. Ten patients (group C) presented urticaria and/or the appearance of angioedema during or 24 h after challenge, with reactions to ASA (five patients) or food additives (five patients). We recruited 15 healthy volunteers as controls (group A). During a second challenge, groups B and C were challenged double-blind with a single dose of ASA, or a specific food additive, or placebo. The healthy group was challenged only with a placebo (talc capsule). Patients in groups B and C were challenged twice: with placebo (as groups B1 and C1) and with ASA (groups B2 and C2) or food additives (C2). Four samples of urine were collected; one during the night before the specific or sham challenge (baseline), and three at 2, 6 and 24 h after the challenge. Urinary methylhistamine (N-MH) and LTE4 were analyzed and normalized for urinary creatinine.
For urinary N-MH at baseline, there was a significant difference only between group A and groups B1, B2, C1 and C2 (A vs. B1, P < 0.0001; A vs. B2, P < 0.0001; A vs. C1, P < 0.0001; A vs. C2, P < 0.0001). We detected a significant variation in urinary methylhistamine excretion only in group C2 after 2 h, 6 h and 24 h (P < 0.0001). However, no variations were observed in N-MH excretion rate in the other groups (A, B1, C1) after challenge with placebo, and in B2 after challenge with ASA 20 mg. For urinary LTE4 at baseline no differences were found between the mean values for the different groups. After specific challenge, only C2 patients showed significantly increased excretion rates of urinary LTE4 compared with the other groups challenged with placebo (A, B1, C1), or ASA (B2) (P < 0.0001). No significant correlation was seen between urinary LTE4 and methylhistamine excretion rate in any patients.
Our results show that urinary excretion of N-MH and LTE4 is different for CU patients without ASA or food hypersensitivity, compared to those with CU with ASA or food additive hypersensitivity after specific challenge.
从尿液中回收介质代谢物有可能提供一种快速、安全且易于获取的介质释放指标。我们旨在确定慢性荨麻疹（CU）患者尿液中的组胺和白三烯（LTs）代谢物。
对20例CU患者进行研究。他们是根据乙酰水杨酸（ASA）和食品添加剂的双盲安慰剂对照激发试验（DBPC）入选的。10例患者（B组）对两种激发试验均呈阴性。10例患者（C组）在激发试验期间或之后24小时出现荨麻疹和/或血管性水肿，对ASA（5例患者）或食品添加剂（5例患者）有反应。我们招募了15名健康志愿者作为对照（A组）。在第二次激发试验中，B组和C组双盲接受单剂量ASA、特定食品添加剂或安慰剂激发。健康组仅接受安慰剂（滑石胶囊）激发。B组和C组患者接受两次激发：接受安慰剂（作为B1组和C1组）以及接受ASA（B2组和C2组）或食品添加剂（C2组）激发。收集四份尿液样本；一份在特定激发试验或假激发试验前一晚（基线），另外三份在激发试验后2、6和24小时。分析尿甲基组胺（N-MH）和LTE4，并根据尿肌酐进行标准化。
对于基线时的尿N-MH，仅A组与B1、B2、C1和C2组之间存在显著差异（A组与B1组比较，P<0.0001；A组与B2组比较，P<0.0001；A组与C1组比较，P<0.0001；A组与C2组比较，P<0.0001）。仅在C2组，激发试验后2小时、6小时和24小时尿甲基组胺排泄量有显著变化（P<0.0001）。然而，安慰剂激发试验后，其他组（A组、B1组、C1组）以及20mg ASA激发试验后的B2组，N-MH排泄率均未观察到变化。对于基线时的尿LTE4，不同组的平均值之间未发现差异。特定激发试验后，与接受安慰剂（A组、B1组、C1组）或ASA（B2组）激发的其他组相比，仅C2组患者尿LTE4排泄率显著升高（P<0.0001）。在任何患者中，尿LTE4与甲基组胺排泄率之间均未发现显著相关性。
我们的结果表明，与特定激发试验后对ASA或食品添加剂过敏的CU患者相比，对ASA或食品不过敏的CU患者尿N-MH和LTE4排泄情况不同。
